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1 Department of Animal Physiology, Lund University, S-223 62 Lund, Sweden; 3 Cardiovascular Research Institute, University of California San Francisco, San Francisco, California 941434-0130; 2 Division of Gastroenterology, Johns Hopkins School of Medicine, Baltimore, Maryland 21205-2195; and 4 Department of Physiology, Northeastern Ohio Universities College of Medicine, Rootstown, Ohio 44272-0095
The contributions of
amiloride-sensitive and -insensitive fractions of alveolar fluid
clearance in adult ventilated rats were studied under control
conditions and after 
-adrenergic stimulation. Rats were
instilled with a 5% albumin solution containing terbutaline (10
4 M) or dibutyryl-cGMP (DBcGMP; 104
M) with or without the cyclic nucleotide-gated cation channel inhibitor
l-cis-diltiazem (103 M) and/or
amiloride (103 M). Alveolar fluid clearance over 1 h
was 18 ± 2% in controls. In controls, amiloride inhibited
46 ± 15% of alveolar fluid clearance, whereas
l-cis-diltiazem had no inhibitory effect.
Terbutaline and DBcGMP stimulated alveolar fluid clearance by 85 ± 3 and 36 ± 5%, respectively. Amiloride and
l-cis-diltiazem inhibited nearly equal fractions
of terbutaline-stimulated alveolar fluid clearance when given alone.
Amiloride and l-cis-diltiazem given together inhibited a significantly larger fraction of alveolar fluid clearance in terbutaline-stimulated rats and in DBcGMP-stimulated rats. Based on
these data, terbutaline stimulation recruited both amiloride-sensitive and l-cis-diltiazem-sensitive pathways. In
contrast, DBcGMP mainly recruited
l-cis-diltiazem-sensitive pathways. Therefore,
the amiloride-insensitive fraction of Na+-driven alveolar
fluid clearance may be partly mediated through cyclic nucleotide-gated
cation channels and activated by an increase in intracellular cGMP.
l-cis-diltiazem; cyclic nucleotide-gated cation channels; dibutyryl-guanosine-3'5'-cyclic monophosphate; epithelial sodium ion channels; terbutaline
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